The objective is to describe the molecular lesions induced in mammalian cells by hyperthermia and determine which of these lesions result in cell lethality and/or delay in cell cycle progression. More specifically, differentiate between heat-induced lesions which in themselves cause cell cycle delay and those which radiosensitize the cells by interacting with x-ray-induced lesions. The general aim is to determine for mammalian cells the molecular mechanism by which heat: 1) kills, 2) causes cell cycle delay and 3) radiosensitizes the cells. The general approach is to search for a correlation between the number of ultrastructural and molecular lesions and both the frequency of chromosomal aberrations and cell lethality when cells are treated in different parts of the cell cycle. The end points to be investigated are: radiation-induced single strand breaks in DNA and the delay and extent of their rejoining, beta polymerase activity as a function of time after heating, effects on repair replication of x-ray damage, changes in the amount and types of chromosomal proteins associated with DNA, damage to the plasma membrane and the mitotic apparatus, and hyperthermic effects on the damage to the plasma membrane and the mitotic apparatus, and hyperthermic effects on the assembly competence of actin contained in microfilaments.